• A Data-Mining Strategy That Identifies Drugs and Genes Associated With Anti-Cancer Drug Sensitivity

      Schleifer, Robert John; Department of Pharmacology and Toxicology (2017)
      The success of cancer therapy for patients often hinges on the responsiveness of the cancer cells to therapeutics. Drug resistance to anti-cancer therapeutics, both intrinsic and acquired, has important clinical and scientific significance. Identification of drug resistance genes using traditional methodologies and translation of those findings to the clinic has proven challenging. We developed a predictive data mining-based bioinformatic framework using public patient data and high-throughput cancer cell drug screening data. This information was used for genome-wide rankings of putative drug resistance genes. Prominent drug resistance genes (e.g. ABCB1, EGFR, and AXL) were successfully identified by the pipeline, additional genes hypothesized to be novel drug resistance genes were then investigated. Experimental confirmation of the novel genes using knockdown technologies indicated a propensity for of decreased proliferation/viability of cancer cells and increased sensitivity for anticancer compounds after knockdown much like known drug resistance genes. We then assessed the potential of each gene as an anti-cancer therapeutic target by exploring how gene knockdown behaved with clinical anticancer compounds. A second arm of the data-mining pharmaco-genomic strategy involved identification of candidate compounds that decrease expression of drug resistance genes. Using the drug resistance gene AXL as a proof-of-concept, three compounds were identified that decreased AXL expression at sub-micromolar concentrations. These compounds were characterized using microarray and cell signaling studies and found to decrease cell cycle signaling as well as activity of the Akt, mTOR, and ERK pathways. This study illustrates a novel approach for rapid and efficient identification of drug sensitivity genes or gene expression altering compounds utilizing bioinformatic data-mining.
    • Deciphering mechanisms of DNA methylation regulation by depletion of the DNA methyltransferases and SETD2

      Tiedemann, Rochelle Lee; Department of Biochemistry and Molecular Biology / Cancer Center (2015)
      DNA methylation (5mC) is a stabile epigenetic mark that confers differential function for gene expression and chromatin accessibility dependent on the context and locality of the mark. Promoter regions populated by CpG islands (CGIs) are highly unmethylated while the remaining ∼80% of CpGs are methylated and distributed across gene bodies, repetitive and transposable elements, and intergenic regions of the genome. The presence and/or absence of particular histone modifications also dictate the patterning of 5mC genome-wide. In cancer, a reversal of 5mC patterns occur in which hypermethylation of tumor suppressor gene CGIs confers gene silencing, and hypomethylation of repetitive and transposable elements contribute to genomic instability. The mechanisms by which 5mC becomes aberrantly regulated in cancer remain unknown. In this study, direct and indirect mechanisms of 5mC regulation were investigated. To understand the direct regulation of 5mC genome-wide, we depleted cell line models of the DNA methyltransferases (DNMTs) that are responsible for establishing (DNMT3A, DNMT3B, DNMT3L) and maintaining (DNMT1) 5mC patterns. Profiling of 5mC patterns on the Illumina HumanMethylation450 BeadChip revealed a unique antithetical relationship between DNMT1 and DNMT3B for the regulation of both 5mC and DNA hydroxymethylation (5hmC) across gene bodies. DNMT3B mediated nonCpG methylation, while DNMT3L influenced the activity of DNMT3B toward nonCG versus CpG site methylation. DNMT3B depletion induced 5mC patterns that closely resemble those observed during cellular differentiation and occurred across gene bodies of highly expressed, H3K36me3-marked genes. SETD2, the histone methyltransferase responsible for H3K36me3 establishment across active gene bodies, was determined to influence the guidance of DNA methylation genome-wide through an indirect mechanism. SETD2 knockout induced widespread loss of H3K36me3 that did not coincide with changes in 5mC. However, paradoxical gains in H3K36me3 significantly induced hypermethylation and upregulation of underlying genes. Genes marked exclusively by the poised enhancer mark, H3K4me1, were commonly targeted for this epigenetic phenotype. DNA methylome profiling of loss-of-function SETD2 mutated clear cell renal cell carcinoma, papillary renal cell carcinoma, and lung adenocarcinoma tumors confirmed the predominance of the hypermethylation phenotype upon loss of SETD2. Collectively, these studies provide novel insight to understanding the regulatory mechanisms by which 5mC patterns are conferred.
    • Decreased expression of Sprouty2 in the dorsolateral prefrontal cortex in schizophrenia and bipolar disorder: a correlation with BDNF expression.

      Pillai, Anilkumar; Department of Psychiatry and Health Behavior (2008-03-12)
      BACKGROUND: Current theories on the pathophysiology of schizophrenia suggest altered brain plasticity such as decreased neural proliferation and migration, delayed myelination, and abnormal synaptic modeling, in the brain of subjects with schizophrenia. Though functional alterations in BDNF, which plays important role in neuroplasticity, are implicated in many abnormalities found in schizophrenia, the regulatory mechanism(s) involved in the abnormal signaling of BDNF in schizophrenia is not clear. The present study investigated whether Sprouty2, a regulator of growth factor signaling, is abnormally expressed in schizophrenia, and is associated with the changes in BDNF mRNA in this disorder. The potential effect of antipsychotic drugs on Sprouty2 expression was tested in adult rats. METHODS AND FINDINGS: Sprouty2 and BDNF gene expression were analyzed in dorsolateral prefrontal cortex samples from the Stanley Array Collection. Quantitative real-time PCR analysis of RNA in 100 individuals (35 with schizophrenia, 31 with bipolar disorder, and 34 psychiatrically normal controls) showed significantly decreased expression of Sprouty2 and BDNF in both schizophrenia and bipolar disorder. Moreover, a significant correlation between these two genes existed in control, schizophrenia and bipolar subjects. Long-term treatment with antipsychotic drugs, haloperidol and olanzapine, showed differential effects on both Sprouty2 and BDNF mRNA and protein levels in the frontal cortex of rats. CONCLUSION: These findings demonstrating decreased expression of Sprouty2 associated with changes in BDNF, suggest the possibility that these decreases are secondary to treatment rather than to factors that are significant in the disease process of either schizophrenia and/or bipolar disorder. Further exploration of Sprouty2-related signal transduction pathways may be helpful to design novel treatment strategies for these disorders.
    • The Defamiliarization of Reality: Redefining Fantasy through a Stationary and Expansionary Model"

      Baggett, Jacob; Department of English and Foreign Languages (Augusta University, 2015-05)
      J.R.R Tolkien’s The Lord of the Rings set the standard for what is now called fantasy literature in an essay entitled “On Fairy Stories.” Tolkien defines fantasy as occurring entirely in a separate “secondary world”. Contemporary fantasy, however, has evolved beyond the scope of Tolkien’s theory by including stories in which the secondary world and the primary world, the world in which we live, are more thoroughly connected. This occurs through a sense of defamiliarization: readers live in the primary world, but as the plot unfolds, they realize that a secondary fantasy world is all around them, previously unfamiliar and unseen. This thesis articulates a new theory of Stationary and Expansionary Fantasy, providing a more inclusive definition of fantasy and integrating the defamiliarization that has become integral to contemporary fantasy. I compare two traditional examples of fantasy, Tolkien’s The Lord of the Rings and Edmund Spenser’s The Faerie Queene, as well as one contemporary example, Susan Cooper’s The Dark is Rising, in order to test the theory and demonstrate its operation in fantasy literature.
    • DEFINING THE ROLE OF TROPOMYOSIN-1C IN CARGO TRANSPORT IN DROSOPHILA

      Boggupalli, Shankarappa Devi Prasad; Department of Cellular Biology and Anatomy (Augusta University, 2020-05)
      Cell polarity is the asymmetric organization of different organelles in a cell, including the plasma membrane and cytoskeleton. Such organization results from asymmetric sorting of proteins, either post-translationally or pre-translationally by messenger RNA localization. In Drosophila oocytes, posterior localization of oskar mRNA is required for germplasm assembly and establishing antero-posterior polarity. oskar mRNA is transported by Kinesin, however the adaptor that links Kinesin to oskar mRNA was not known. In Aim 1 of this thesis, we demonstrate that a novel isoform of Tropomyosin, namely Tm1C, binds directly to kinesin and functions as the adaptor in linking kinesin to oskar mRNA. Oskar expression is limited to female germline, however Tm1C is also expressed in male flies. This suggests that there might be additional cargoes for Tm1C. We attempted to identify novel cargoes of Tm1C by performing a proteomic assay in Drosophila S2 cells. Apart from Khc, we identified Supernumerary limbs (Slmb) as the main interacting partner. Our further investigation of Slmb suggests that it might not be a cargo. Instead, Slmb which is a component of E3 ubiquitin ligase, might regulate the expression of Tm1C. In Aim 2 of the thesis, we show that Slmb regulates the levels of Tm1C by ubiquitinating it and facilitating its degradation by the Proteasome.
    • Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines.

      Kimura, Yasutoshi; Takada, Tadahiro; Kawarada, Yoshifumi; Nimura, Yuji; Hirata, Koichi; Sekimoto, Miho; Yoshida, Masahiro; Mayumi, Toshihiko; Wada, Keita; Miura, Fumihiko; et al. (2007-01-25)
      This article discusses the definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis. Acute cholangitis and cholecystitis mostly originate from stones in the bile ducts and gallbladder. Acute cholecystitis also has other causes, such as ischemia; chemicals that enter biliary secretions; motility disorders associated with drugs; infections with microorganisms, protozoa, and parasites; collagen disease; and allergic reactions. Acute acalculous cholecystitis is associated with a recent operation, trauma, burns, multisystem organ failure, and parenteral nutrition. Factors associated with the onset of cholelithiasis include obesity, age, and drugs such as oral contraceptives. The reported mortality of less than 10% for acute cholecystitis gives an impression that it is not a fatal disease, except for the elderly and/or patients with acalculous disease. However, there are reports of high mortality for cholangitis, although the mortality differs greatly depending on the year of the report and the severity of the disease. Even reports published in and after the 1980s indicate high mortality, ranging from 10% to 30% in the patients, with multiorgan failure as a major cause of death. Because many of the reports on acute cholecystitis and cholangitis use different standards, comparisons are difficult. Variations in treatment and risk factors influencing the mortality rates indicate the necessity for standardized diagnostic, treatment, and severity assessment criteria.
    • Deletion of the Mammalian Homolog of Yeast Vacuolar Protein Sorting 34 Inhibits Compensatory Nephron Hypertrophy

      Liu, Ting; Department of Cellular Biology and Anatomy (2016-03)
      Reduction of functioning nephrons stimulates all components of the remaining nephrons, particularly the proximal tubule, to undergo compensatory nephron hypertrophy (CNH). Recent studies in our lab revealed activation of the mammalian homolog of yeast vacuolar protein sorting 34 (mVPS34) in the remaining kidney within 30 min in response to uninephrectomy (UNX). Interestingly, mVPS34 has been reported to be an upstream mediator of mTORC1 activation in cultured cells. However, whether mVPS34 activation is essential in mediating mTORC1 signaling to CNH in vivo remains unknown. We crossed mVPS34flox/flox mice with SG.Cre mice expressing tamoxifen-inducible Cre recombinase mainly in the S1 and S2 segments of the proximal tubule and generated proximal tubule-specific mVPS34 knockout (mVPS34ptKO) mice. The body weight and kidney/body weight ratio (K/Bwt) of mVPS34ptKO mice were similar to those of wild type control (mVPS34Ctrl) littermates. 8-week-old mVPS34Ctrl and mVPS34ptKO mice were uninephrectomized. UNX-induced CNH in mVPS34ptKO mice was blocked by 40-55%, as indicated by inhibition of increases in K/Bwt ratio compared to that of mVPS34Ctrl mice (15.81±2.82 vs. 33.15±1.97%; p<0.001, n=7-9). There was no change in BUN levels in mVPS34ptKO and mVPS34ctrl mice with or without UNX. This study provided the first genetic evidence that mVPS34 mediates 40-55% of CNH. Further studies will determine the interactions between mVPS34 activation and mTORC1 signaling in regulating CNH.
    • Delusional Disorder in the Narrator of Maud

      Ravula, Havilah; English and Foreign Languages (Augusta University Libraries, 2020-05-04)
      This item presents the abstract for an oral presentation at the 21st Annual Phi Kappa Phi Student Research and Fine Arts Conference.
    • Dendritic Cell Derived Exosomes Loaded with Immunoregulatory Cargo Reprogram local Immune Responses and Inhibit Degenerative Bone Disease In vivo

      Elashiry, Mahmoud; Biomedical Sciences (Augusta University, 2020-12)
      Background: Histopathological study of periodontitis (PD) lesions at sites of bone loss reveals infiltration with dendritic cells (DC) CD4+ T cell clusters and other inflammatory cells. DCs can direct bone protective T-regulatory cell (Tregs) responses, or bone destructive T-helper 17 (Th17). The use of exosomes (EXO), natural nanoparticles released by DCs and other cells, are under intense scrutiny in clinical trials for autoimmune diseases and cancer, but no studies to date have harnessed DC-derived EXO to regulate alveolar bone loss in PD. Aim: To determine the ability of custom DC-derived EXO to reprogram immune cell functions of recipient DCs and T cells and mitigate inflammatory bone loss in mice. Methods: Murine bone marrow derived donor DC subtypes, including immune regulatory DCs (regDC), immature DCs (iDC) and immune stimulatory (stimDC) DCs were the source of purified DC EXO. Reg DC EXO were actively loaded with TGFB1/IL10 using ultrasonication. Preliminary in vitro studies of EXO cargo, stability and resistance of cytokine cargo to proteolysis, as well as immune functions and osteoclastogenesis was investigated. The following DC EXO subtypes were then tested in vivo in six groups of mice, in the ligature induced PD model: Group 1, no ligature, Groups 2, 3, 4, 5 and 6, 8 ligature plus gingival injection of, respectively, PBS, regDC EXO, iDC EXO, stimDC EXO and free TGFB1/IL10. Biodistribution and in vivo uptake of EXO by gingival recipient DCs and T cells were tracked. The ability of DC EXO to modulate gingival recipient DC and CD4 T cells and cytokine expression was confirmed. TRAP staining of histological sections measured osteoclast number, while bone loss volume was measured in 3-D by micro-CT. Results: Injected EXO showed a high affinity for gingival site of inflammatory bone loss. RegDC EXO containing TGFb/IL-10 cargo, protected cargo against proteolytic degradation and were taken up by recipient DCs and T cells in vivo, promoting Tregs, while inhibiting Th17 recruitment and inhibiting bone loss. In contrast, EXO subtypes lacking TGFb/IL-10 or free TGFB/IL-10 did not shift the Treg-Th17 balance and did not inhibit bone loss. Mechanistically, a key role for TGFb1 in induction of Tregs by regDC EXO was found using blocking antibodies to TGFb and/or IL-10. T.E.M. analysis revealed TGFb1 localized in the EXO lumen and in the transmembrane domain, which sustained signaling in recipient DCs. Blocking experiments revealed that sustainable prolonged TGFb1 signaling required initial interaction between regDCs EXO and TGFBR1 complex on acceptor cells, followed by internalization of regDC EXO with TGFB1-TGFBR1 complex for sustained SMAD2/3 phosphorylation. Conclusion: This is the first study to demonstrate the efficacy of DCs exosomes for inhibition of experimental bone loss and the cellular immune mechanisms involved. This provides the basis for a future novel immunotherapeutic strategy for PD in humans.
    • Dentin Sialophosphoprotein (DSPP) Gene-Silencing Inhibits Key Tumorigenic Activities in Human Oral Cancer Cell Line, OSC2

      Joshi, Rajeshree; Tawfik, Amany; Edeh, Nneka; McCloud, Veronica; Looney, Stephen W.; Lewis, Jill; Hsu, Stephen; Ogbureke, Kalu U.E.; Department of Oral Biology; Department of Pathology; et al. (2010-11-12)
      Background: We determined recently that dentin sialophosphoprotein (DSPP), a member of the SIBLING (Small integrin-binding ligand N-linked glycoproteins) family of phosphoglycoproteins, is highly upregulated in human oral squamous cell carcinomas (OSCCs) where upregulation is associated with tumor aggressiveness. To investigate the effects of DSPP-silencing on the tumorigenic profiles of the oral cancer cell line, OSC2, short-hairpin RNA (shRNA) interference was employed to silence DSPP in OSC2 cells.
    • Design & Synthesis of Pyrazinamide Hybrid Conjugates as Potential Anti-tubercular Agents

      Torkian,Behrad; Panda, Siva S.; Department of Chemistry & Physics (2017-03)
      Tuberculosis (TB) is a bacterial pathogen caused by Mycobacterium tuberculosis, which generally causes pulmonary infection and is extremely pervasive within the lungs and between subjects. Pyrazinamide (PZA) is a first-line prodrug used synergistically with two or more chemotherapies to eradicate TB. PZA is hydrolyzed to its active constituent, pyrazinoic acid, intracellularly in M. tuberculosis via pyrazinamidase. With prolonged administration of the recommended dose, harmful side effects have been reported: hepatitis, acute hypertension, thrombocytopenia, and gastrointestinal discomfort Drug-amino acid conjugates are used because of increased tissue delivery, in which the amino acids act as effective carriers of these agents while maintaining, and even amplifying, their bioactive integrity. Amino acid conjugates can increase bioavailability and quantitatively decrease the required amount of active drug thus preventing toxic side effects. We have synthesized several pyrazinamide conjugates with secondary amines via amino acid linkers with retention of chiral integrity of the desired products. Secondary amines are known for enhancing biological properties of various potential molecules. All the synthesized compounds were characterized by NMR and X-ray studies. The synthesized conjugates are expected to have better anti-tubercular properties with less side effects.
    • Design and Manufacture of Low-Cost Real-Time Feedback CPR Manikin

      Sangari, Anish; Sood, Nitish; Department of Chemistry & Physics; Augusta University (2019-02-13)
      Cardiopulmonary Resuscitation (CPR) is a life-saving technique used when a person stops breathing or a heart stops beating. Immediate CPR can double or triple survival rates after cardiac arrest. While many CPR training courses use non-electronic CPR manikins, recent literature has shown that training on a real-time feedback CPR manikin improves functional outcomes such as chest compression rate and mean tidal volume. However, current commercially available real-time feedback manikins either only measure metrics on chest compressions or are available at very high prices, making training a class on such manikins infeasible. Accordingly, we have designed, constructed, and tested a low-cost Arduino microcontroller-based CPR manikin that provides real-time feedback to trainees on critical metrics including force of compressions, rate of compressions, hands-off time, percentage of full chest recoils, angle of neck tilt, and other steps in ventilations. Visual and auditory feedback on these metrics is delivered to trainees, allowing them to adjust their performance in real time. Additionally, data from each training session is saved and assigned to a user profile, so that multiple trainees can review their progress throughout their training. Future research will be conducted on the efficacy of training on this manikin compared to commercially available manikins.
    • DESIGN AND SYNTHESIS OF HYBRID CONJUGATES AS POTENTIAL ANTI-INFECTIVE AGENTS

      Littlefield, William E; Wade, Margaret; Makkanal, Tina; College of Science and Mathematics; Department of Chemistry and Physics; Panda, Silva; Augusta University (2019-02-13)
      Infectious diseases caused by pathogenic microorganisms are major challenges despite all the steps taken to control or cure. New drug development with high efficacy/selectivity for infectious diseases is a point of interest for many researchers. It has reported that tuberculosis is one of the ten major causes of death in the world. Multi-drug resistance (MDR) is another major concern in bacterial and fungal infections. The present study deals with the development of new conjugates of pyrazinoic acid and isoniazid linked via an amino acid. The synthesized conjugates show promising and interesting results against a variety of microbial strains, tuberculous and non-tuberculous mycobacteria. Molecular modeling studies were used for understanding and validation of the experimental data.
    • Design and Synthesis of Metformin Derivatives as Anticancer Agents

      Thomas, Eyana; Department of Biological Sciences (Augusta University, 2021-05)
      Metformin is the first-line medication for type II diabetes. It initially entered the spotlight as a promising anti-cancer agent due to epidemiologic reports that reduced cancer risk and improved clinical outcomes in diabetic patients taking Metformin. To uncover the anti-cancer mechanisms of Metformin, preclinical studies determined that Metformin impairs cellular metabolism and suppresses oncogenic signaling pathways. Recently, the anti-cancer potential of Metformin has gained increasing interest due to its inhibitory effects on cancer stem cells (CSCs), which are associated with tumor metastasis, drug resistance, and relapse. There is a need to optimize this drug to target a more general audience of non-diabetic cancer patients. Metformin has low bioavailability, a narrow absorption window, and extensive liver metabolism. Its oral administration is accompanied by gastrointestinal adverse effects, including nausea, abdominal pain, abdominal bloating, flatulence, dyspepsia, and anorexia, resulting in up to 50% of patients. We have synthesized metformin hybrid conjugates with aromatics compounds. Spectral studies characterized all the synthesized compounds. The hybrid conjugates showed improved LogP values, determined from computational analyses, over tenfold of Metformin's 0.15, suggesting that these candidates will show better bioavailability in the body.
    • Design and Synthesis of Novel NSAID Hybrid Conjugates as Potential Anti-inflammatory

      Honkanadavar, Hitesh; Department of Chemistry and Physics (Augusta University, 2019-05)
      Non-steroidal anti-inflammatory drugs are one of the most common drugs administered worldwide as highly effective analgesic, antipyretic and anti-inflammatory agents. The drugs function by inhibiting the COX-2 enzyme system which leads to a decrease in inflammation; however, the drugs also inhibit the COX-1 enzyme system which is critical to maintaining the integrity of the stomach lining as well as proper kidney function. Inhibition of this enzyme system can lead to stomach ulcers and kidney dysfunction. Hybrid conjugates of existing non-steroidal anti-inflammatory drugs (NSAIDs) have already been synthesized with ibuprofen, acetaminophen, and amino acids to increase potency and decrease toxicity. Computational chemistry studies of these compounds show that the free phenol moiety in acetaminophen plays a greater role in the inhibition of the COX-2 enzyme system than the amine moiety. The previous compounds utilized the phenol moiety to form the product. New hybrid conjugates of ibuprofen and acetaminophen via amino acid linkers have been synthesized, leaving the phenol moiety free. The compounds have been characterized by nuclear magnetic resonance and infrared spectroscopy. Biological studies indicate that some of the synthesized compounds are showing improved potency when compared to ibuprofen alone as well as decreased ulcer formation.
    • DESIGN AND SYNTHESIS OF QUINOLONE-TRIAZOLE CONJUGATES AS POTENTIAL ANTIBACTERIAL AGENTS

      Honkanadavar, Hitesh H; Tran, Queen; Department of Chemistry and Physics; Panda, Silva; Augusta University (2019-02-13)
      Quinolones are one of the most important synthetic antibacterial agents have been widely used in the treatment of diverse infections including urinary tract, respiratory and bone joint as well as sexually transmitted diseases, prostatitis, pneumonia, and acute bronchitis. However, quinolone resistance increases towards many Gram-negative and Gram-positive species. Molecular conjugation has been known for the rational design of new biologically active entities by fusion of compounds and/or pharmacophores recognized and derived from known bio-active molecules. The present study directs towards the construction of novel quinolone-triazole conjugates and investigation of their antimicrobial properties. The detail results will be discussed at the conference.
    • Design and Synthesis of Selective COX-2 Inhibitors as Potential Anti-Inflammatory Agents

      Wade, Margaret; Chemistry and Physics (Augusta University Libraries, 2020-05-04)
      This item presents the abstract for an oral presentation at the 21st Annual Phi Kappa Phi Student Research and Fine Arts Conference.
    • Design, Synthesis, and Anti-inflammatory Studies of NSAID Hybrid Conjugates

      Honkanadavar, Hitesh; Department of Chemistry & Physics; Panda, Siva; Augusta University (2019-02-13)
      Non-steroidal anti-inflammatory drugs are one of the most common drugs administered worldwide as highly effective analgesic, antipyretic and anti-inflammatory agents. The drugs function by inhibiting the COX-2 enzyme system which leads to a decrease in inflammation; however, the drugs also inhibit the COX-1 enzyme system which is critical to normal renal function, gastric mucosal integrity, vascular homeostasis, and the autocrine response to circulating hormones which can lead to gastric ulcers and renal dysfunction. Hybrid conjugates of existing non-steroidal anti-inflammatory drugs (NSAIDs) have already been synthesized with Ibuprofen, Acetaminophen, and amino acids to increase potency and decrease toxicity. Computational chemistry studies of these compounds show that the free phenol moiety in acetaminophen plays a greater role in the inhibition of the COX 2 enzyme system than the amine moiety. The previous compounds utilized the phenol moiety to form the product. New hybrid conjugates of Ibuprofen and Acetaminophen via amino acid linkers have been synthesized, leaving the phenol moiety free. The compounds have been characterized by NMR and IR. Biological studies indicate that some of the synthesized compounds are showing improved potency when compared to Ibuprofen alone. Computational chemistry studies and molecular modeling will be used to support the�in-vivo�biological activity.
    • Design, Synthesis, and Computational Studies of Isoniazid Hybrid Conjugates as Potential Antimycobacterial Agents

      Thomas, Eyana; Chemistry and Physics (Augusta University Libraries, 2020-05-04)
      This item presents the abstract for an oral presentation at the 21st Annual Phi Kappa Phi Student Research and Fine Arts Conference.